Evidence map›Paper›PMID 40082348›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Current Methodologies to Assess Cellular Senescence in Cancer.

Panayiotis Laouris, Daniel Muñoz-Espín

Abstract read
PubMed Publisher
In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Panayiotis LaourisEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK.
Daniel Muñoz-EspínEarly Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, UK. dm742@cam.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence plays a critical role in cancer, acting as both a tumor-suppressive and tumor-promoting mechanism. Senescent cells undergo stable cell-cycle arrest in response to various stressors, including DNA damage and oncogenic signaling, and exhibit a complex secretory phenotype known as the senescence-associated secretory phenotype (SASP), which can impact the tumor microenvironment. The hallmarks of senescence include cell-cycle arrest, secretion of pro-inflammatory factors, structural changes, and metabolic alterations. These features, while initially suppressing tumorigenesis, can later contribute to cancer progression under certain conditions. Methods for studying senescence in preclinical models include in vitro assays, ex vivo tissue analysis, and in vivo detection techniques. Emerging therapeutic strategies focus on exploiting senescence for cancer treatment, particularly through the use of senolytic agents that selectively eliminate senescent cells and senomorphic compounds that modulate SASP activity. However, the identification of reliable and universal biomarkers for senescence remains a challenge, necessitating a multimarker approach to accurately detect and characterize senescent cells in various contexts.

Indexed as

Cellular SenescenceNeoplasmsAnimalsDNA DamageHumansSenescence-Associated Secretory PhenotypeTumor MicroenvironmentBiomarkersCancerCellular senescenceMethodologiesOncogene-induced-senescence

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.